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Flashcards in Cardio Drugs Deck (44):
1

Calcium Channel Blockers - names

amlodipine, nimodipine, nifedipine (dihydropyridine), diltiazem, verapamil (non-dihydropyridine)

2

CCB mechanism of action

block voltage-dependent L-type calcium channels of cardiac and smooth muscle, thereby reducing muscle contractility
- vascular smooth muscle -- amlodipine = nifedipine > dilt > verapamil
- heart -- verapamil > dilt > amlodipine = nifedipine
- verapamil likes the ventricle

3

CCB clinical use

dihydropyridine (except nimodipine): HTN, angina, Raynaud
non-dyhydropyridine: HTN, angina, afib/flutter
Nimodipine: SAH (prevents cerebral vasospasm)

4

CCB toxicity

cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia and constipation

5

hydralazine mechanism

increases cGMP --> smooth muscle relaxation. vasodilates arterioles > veins; afterload reduction

6

hydralazine clinical use

severe HTN, CHF. first line therapy for HTN in preggos, with methyldopa. frequently co-administered with a beta blocker to prevent reflex tachycardia

7

hydralazine toxicity

compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina.
**Lupus like syndrome (due to liver acetylation of the drug)

8

Drugs to treat hypertensive emergency

nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam
- Neil likes Neil's fun clonipine

9

nitroprusside

short acting, increases cGMP via direct release of NO. can cause cyanide toxicity (releases cyanide)

10

fenoldopam

dopamin D1 receptor agonist - coronary, peripheral, renal and sphlanchnic vasodilation. Decreases B and natriuresis

11

nitroglycerin, isosorbide mononitrate mechanism

vasodilate by increasing NO in smooth muscle --> increases cGMP and smooth muscle reladation. dilates veins >> arteries, decreases preload

12

clinical use of nitro/isosorbide mononitrate

angina, ACS, pulmonary edema

13

toxicity of nitro/isosorbide mononitrate

reflex tachycardia (treat with beta blockers), hypotension, flushing, headache
"Monday disease" - lack of use over the weekend causes lack of tolerance, more side effects on reexposure

14

niacin effects on LDL, HDL and TG

significantly decreases LDL, significantly increases HDL, decreases TG
**best for increasing HDL

15

bile acid resins effects on LDL, HDL and TG

significantly decrease LDL, slightly increases HDL and TG

16

HMG CoA reductase inhibitors effects on LDL, HDL and TG

significantly decreases LDL, increases HDL and decreases TG
** best for decreasing LDL

17

cholesterol absorption blockers effects on LDL, HDL and TG

significantly decreases LDL, no effect on HDL/TG

18

fibrates effects on LDL, HDL and TG

significantly decreases TG, decreases LDL and increases HDL
** best at decreasing TG

19

niacin mechanism of action and SE

- inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis
- SE: flushing (dec by aspirin, long term use), hyperglycemia, hyperuricemia

20

HMG CoA reductase mechanism of action and SE

inhibits conversion of HMG CoA --> mevalonate, a cholesterol precursor
- increase LDL receptor density
- hepatotoxic, rhabdo

21

bile acid resins mechanism of action and SE

- prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more
- tastes bad, GI discomfort, decreased absorption of fat-soluble vitamins, cholesterol gallstones

22

cholesterol blockers mechanism/SE

- blocks absorption at the small intestine brush border
- rare inc in LFTs, diarrhea, hepatotox when given with statins

23

fibrates mech of action/SE

-upregulate lipoprotein lipase, increase TG clearance
- activates PPARalpha to induce HDL synthesis
- suppresses 7alpha hydroxylase
- myositis, hepatotoxicity, cholesterol gallstones (esp with bile acid resins)

24

Digoxin pharmacokinetics

- 75% bioavailability
- 20-40% protein bound
- t 1/2 = 40 hours
- urinary excretion

25

digoxin mechanism and clinical use

- direct inhibition of Na/K ATPase leads to indirect inhibition of the Na/Ca exchanger/antiport
- more Ca means positive intropy
- stimulates vagus nerve --> decreased HR
- used in CHF, afib

26

dig toxicity

- cholinergic - n/v/d, blurry yellow vision
- ECG - increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block
- can lead to hyperK
- precipitators of tox: renal failure, hypoK, verapamil, amiodarone, quinidine
- antidote: normalize K, cardiac pacer, anti-dig Fab fragments, Mg

27

Class 1 antiarrythmics - Na blockers

slow or block conduction, decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells. Hyperkalemia causes increased toxicity for all class I drugs

28

Class 1A antiarrhythmics (names)

Quinidine, Procainamide, Disopyramide
- "Quarter PounDer"

29

Class 1A mechanism/clinical use

increase AP duration, increase effective refractory period, increase QT
- used for both atrial and ventricular arrhythmias, esp re-entrant and ectopic SVT and VT

30

Class 1A toxicity

cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades

31

Class 1B meds

lidocaine, mexiletine, also phenytoin?
"Lettuce and mayo"

32

Class 1B mechanism/use

- decreased AP duration, preferentially affect ischemic or depolarized purkinje/ventricle tissue
- acute ventricular arrhythmias (esp post MI)

33

Class 1B tox

CNS stimulation/depression, CV depression

34

Class 1C meds

flecainide, propafenone
"Can i have Fries Please?"

35

Class 1C mech/use

- significantly prolongs refractory period in AV node
- minimal effect on AP duration
- used in SVTs, including afib. only as a last resort in refractory VT

36

Class 1C toxicity

proarrhythmic, esp post-MI (contraindicated)
- fries are contraindicated post-MI

37

Class 2: beta blockers (names) and mechanism and use

metoprolol, propranolol, esmolol (short-acting), atenolol, timolol, carvedilol
- decrease SA and AV node activity by decreaseing cAMP and Ca currents. supress abnormal pacemakers by decreasing the slope of phase 4
- AV node particularly sensitive - inc PR
- used in SVT, afib and aflut

38

beta blocker toxicity

impotence, exacerbation of COPD and asthma, bradycardia, AV block, CHF, sedation, sleep alterations
- may mask the signs of hypoglycemia
- metop can cause dyslipidemia
- prop can exacerbate vasospasm of P. angina
- contraindicated in cocaine users
- treat overdoses with glucagon

39

Class III antiarrhythmics - K channel blockers mech and use

amiodarone, ibutilide, dofetilide, sotalol (AIDS)
- increase AP duration, inc ERP, used when other antiarrhythmics fail. increase QT!
- used in afib, aflut, Vtach (amiodarone, sotalol)

40

K channel blockers tox

- sotalol - torsades, excessive B blockade
- ibutilide - torsades
- amiodarone - LOW risk torsades, pulm fibrosis, hepatotoxic, thyroid up or down, corneal deposits, photodermatitis, neuro, constipation, CHF, bradycardia, heart block

41

Class IV antiarrhythmics - Ca channel blockers

verapamil, diltiazem (non-dihydropyridine)
- decrease conduction velocity, increased ERP, inc PR
- prevent nodal arrhythmias (SVT), rate control of afib

42

Ca channel blocker tox

constipation, flushing, edema, AV nodal block, CHF

43

adenosine

increases K out of cells, hyperpolarizes cell and decreases ICa
- drug of choice for diagnosing/abolishing SVT
- lasts 15 sec
- SE: flushing, hypotension, chest pain
- effects blocked by thephylline and caffeine

44

Mg2+

effective in torsades and dig tox